Because β-cell mass was not reduced in 2.5- and 7.5-month-old Irp2−/− mice, this suggests that phosphorylated eIF2α-mediated translational attenuation may allow Irp2-deficient β cells to adapt to cellular iron deficiency, thereby providing protection against UPR activation of apoptotic signaling pathways. The gene discussed is IREB2; the disease is nutritional disorder.